Conventional approaches to the repair of tissue damage and assisting in the recovery from such damage are not comprehensive and have a number of drawbacks. Thus, tissue damage, and particularly damage to tendons, represents a significant challenge.
Tendons are a form of connective tissue and possess great flexibility and elasticity, which allow forces generated by muscle contraction to be transmitted to the attached bone, enabling movement. As a result of their ability to absorb external forces, tendons are able to act as a buffer, helping to prevent injury to the attached muscle.
Natural tendon is an example of a highly organised hierarchical tissue. It is principally composed of aligned collagen type I fibres with tenocytes arranged in rows between these fibres. Mechanical properties of tendons differ depending on their location within the body. In vivo studies on human Achilles' [Magnusson S P et al 2003] and tibialis anterior [Maganaris C N, 1999] tendons yielded moduli of 788 MPa and 1.2 GPa and tensile strengths 36.5 MPa and 25 MPa respectively. However, testing was not performed to rupture and can only be used as a guide.
All tendons have the potential to be affected by direct damage caused by lacerations or other accidental injuries. They are also susceptible to diseases. Clinically, tendon disorders are referred to as a “tendinopathy” as this makes no assumption as to the pathological processes within the tendon, although the term “tendonitis” is still used.
Of particular concern are tendinopathies within the Achilles tendon, which cause degeneration of the tissue. These are often the result of excessive and repetitive over-loading of the Achilles tendon in both sporting and sedentary patients.
Other tendons prone to pathology include the rotator cuff in the shoulder, where degeneration and the size of tears typically increases with age, and the patella tendon in the knee, which experiences degeneration due to excessive load bearing and strain rather than inflammatory tendinitis.
A variety of treatments are employed for tendinopathy management. In the early phase of disease, conservative methods (such as the use of non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroids) are customarily employed. For those patients who do not respond well to these treatments after 6 months, surgical intervention is common.
For patients presenting acute rupture of the Achilles tendon, treatment falls within three main categories—open operative, percutaneous operative and non-operative.
Open operative surgery involves the repair of the two ruptured ends of the tendon by suturing them together. Percutaneous operative is a combination of open and non-operative techniques and involves a number of small incisions used to suture the tendon without fully exposing the tissue. Non-operative treatments involve the immobilisation of the lower leg in a plaster cast for a period of 6-8 weeks.
Due to the often poor response to treatment, and resultant morbidity of tendon disease, there is a growing interest in novel techniques for repair of such tissues. Following injury, tendon heals by production of scar tissue, which is organisationally, biochemically and biomechanically inferior to normal tendon matrix tissue. Such inferior scar tissue leads to ongoing morbidity of affected patients.
Previous strategies employed to improve the quality of tendon repair after injury include xenograft tendons cross-linked with glutaraldehyde [Smith et al, 1986]. Tissue engineering approaches have utilised autologous tenocytes in biomaterial scaffolds [Cao et al, 2002]. Collagen-based scaffolds have been investigated in an attempt to match the mechanical properties with native tendon [Venugopal et al, 2005 and Curtis et al, 2005].
Synthetic bioresorbable polymers such as polycaprolactone (PCL), polylactic acid (PLA) and chitin have been formed as fibrous mats of randomly orientated fibres, but with limited success (Li et al, 2003).